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Perspective The NEW ENGLAND JOURNAL of MEDICINE 10.1056/nejm p 1007051  nejm.org 1 pathological consequences of trau- matic brain injury has been elevat- ed not only by the recognition of the potential clinical significance of repetitive head injuries in such high-contact sports as American football and boxing, but also by the prevalence of vehicular crash- es and efforts to improve passen- ger safety features, and by modern warfare, especially blast injuries. Each year, more than 1.5 million Americans sustain mild traumat- ic brain injuries with no loss of consciousness and no need for hospitalization; an equal number sustain injuries sufficient to im- pair consciousness but insuffi- ciently severe to necessitate long- term institutionalization. The skull provides the brain with a protective thick, bony en- casement, yet its irregular inte- rior presents opportunities for damage to the fragile tissues it has evolved to protect. Direct mechanical trauma injures corti- cal tissue; traumatic hematomas damage subcortical structures and precipitate vasospasm and ische- mia; and sudden movement of the skull on its vertebral axis pro- duces rotational, acceleration, or deceleration injury, damaging the long axons interconnecting brain regions. Research regarding trau- matic brain injury has long been challenged by the range of these lesions and clinical manifesta- tions, several of which are fre- quently present concurrently. Many complications of trau- matic brain injury are evident im- mediately or soon after injury. Acute post-traumatic sensory, motor, and neurocognitive syn- dromes are presumed to occur as a result of contusions and axonal disruption. Seemingly mild closed- head injuries (i.e., those without skull fracture) may lead to di- verse and sometimes disabling symptoms, such as chronic head- aches, dizziness and vertigo, diffi- culty concentrating, word-finding problems, depression, irritability, and impulsiveness. The duration of such symptoms varies but can be months. Post-traumatic stress disorder frequently accompanies traumatic brain injury, though the relationship is poorly understood. Causal relationships between traumatic brain injury and de- layed sequelae have been less studied because of the variable latency period before overt neu- rologic dysfunction. Severe single- incident injuries, with or with- out skull fracture, may lead to permanent brain damage, with in- complete recovery and residual sensory, motor, and cognitive deficits. If consciousness is lost for more than 30 minutes, the Traumatic Brain Injury — Football, Warfare, and Long-Term Effects Steven T. DeKosky, M.D., Milos D. Ikonomovic, M.D., and Sam Gandy, M.D., Ph.D. I
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This note was uploaded on 10/14/2010 for the course ZOO 4125 taught by Professor Flanigan during the Fall '10 term at Wyoming.

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